Suppr超能文献

长期蓝光照射下视网膜神经节细胞损伤暴露的氧化应激和线粒体功能障碍

Oxidative stress and mitochondrial dysfunction of retinal ganglion cells injury exposures in long-term blue light.

作者信息

Guo Ke-Xin, Huang Chen, Wang Wei, Zhang Pei, Li Ying, Liu Zi-Yuan, Wang Min-Shu

机构信息

Peking University Third Hospital, Beijing 100191, China.

Medical Research Center, Peking University Third Hospital, Beijing 100191, China.

出版信息

Int J Ophthalmol. 2020 Dec 18;13(12):1854-1863. doi: 10.18240/ijo.2020.12.03. eCollection 2020.

Abstract

AIM

To investigate the phototoxic effect of long-term excessive narrow-band blue light in staurosporine-induced differentiated retinal ganglion cells-5 (SSRGC-5).

METHODS

SSRGC-5 cells were divided into two groups, blue light group (BL group) and control group. Cell viability was assessed by using CCK-8 assay. Metabolic profile analysis was performed by using Seahorse extracellular flux analyzer. Mitochondria ultrastructure were studied transmission electron microscope (TEM). Mitochondria contents and oxidative stress was evaluated by flow cytometry. Western blotting was performed to monitor the changes in mitogen-activated protein kinases (MAPK) pathway and PI3K/AKT pathway.

RESULTS

Blue light caused morphological changes of SSRGC-5 cells. The cell viability was significantly decreased from 3h in BL group. Intercellular ROS and mitochondrial superoxide levels were increased following blue light exposure. Metabolic profiling identified blue light induced SSRGC-5 cells to have severely compromised mitochondrial function. This was accompanied by impaired mitochondrial ultrastructure and remodeling, increased expression of the mitochondrial related proteins, and increased glycolysis as compensation. Moreover, the results showed that blue light induced higher expression of p-p38, p38, p-JNK, p-ERK, p-c-Jun, c-Jun, and p-AKT.

CONCLUSION

These findings indicate that excessive narrow-band blue light induces oxidative stress and mitochondrial metabolic remodeling dysregulate in SSRGC-5 cells. Activated MAPK and AKT signaling pathways are involved in this process.

摘要

目的

研究长期过量窄带蓝光对星形孢菌素诱导分化的视网膜神经节细胞-5(SSRGC-5)的光毒性作用。

方法

将SSRGC-5细胞分为两组,蓝光组(BL组)和对照组。采用CCK-8法评估细胞活力。使用海马细胞外流量分析仪进行代谢谱分析。通过透射电子显微镜(TEM)研究线粒体超微结构。通过流式细胞术评估线粒体含量和氧化应激。进行蛋白质印迹法以监测丝裂原活化蛋白激酶(MAPK)途径和PI3K/AKT途径的变化。

结果

蓝光导致SSRGC-5细胞形态发生变化。BL组细胞活力从3小时起显著降低。蓝光照射后细胞内活性氧(ROS)和线粒体超氧化物水平升高。代谢谱分析表明蓝光诱导SSRGC-5细胞的线粒体功能严重受损。这伴随着线粒体超微结构受损和重塑、线粒体相关蛋白表达增加以及糖酵解增加作为补偿。此外,结果显示蓝光诱导p-p38、p38、p-JNK、p-ERK、p-c-Jun、c-Jun和p-AKT的表达升高。

结论

这些发现表明过量窄带蓝光诱导SSRGC-5细胞氧化应激和线粒体代谢重塑失调。激活的MAPK和AKT信号通路参与了这一过程。

相似文献

本文引用的文献

10
Targeting mitochondrial function to protect against vision loss.针对线粒体功能以预防视力丧失。
Expert Opin Ther Targets. 2016 Jun;20(6):721-36. doi: 10.1517/14728222.2015.1134489. Epub 2016 Jan 13.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验